The compound at the center of the study belongs to a family of molecules derived from one of immunology’s most storied discoveries: lipopolysaccharide, or LPS, the toxic component of the outer membrane of gram-negative bacteria. LPS was the first identified agonist of TLR4, a transmembrane signaling receptor expressed on macrophages and dendritic cells that serves as an alarm bell for the innate immune system. Raw LPS, however, provokes dangerous, unregulated inflammation. Scientists therefore developed mimetics of monophosphoryl lipid A (MPLA), the immunostimulatory core of LPS, which retain the receptor-activating power while shedding most of the toxicity. These MPLA-based adjuvants are already embedded in approved human vaccines, including GSK’s AS01 and AS04 formulations, and have been delivered to millions of people.

EmT4™ takes this concept a step further. Rather than a hydrolyzed mixture of acylated lipid species derived from Salmonella bacteria, it contains a single, fully defined synthetic molecule called 3D (6-acyl)-PHAD, the hexaacyl form known to be the active congener in humans. The agonist is incorporated into a squalene-based oil-in-water emulsion stabilized with glycerol and polysorbate 80, with particles of roughly 100 nanometers. Produced under good manufacturing practice conditions in an ISO7 cleanroom, the formulation is functionally analogous to GLA-SE and AS02, adjuvants that have themselves been tested intratumorally in human cancer patients. In mouse studies, EmT4™ proved well tolerated even with daily dosing, boosted the breadth and strength of mRNA vaccine responses against SARS-CoV-2 spike protein, and generated robust protective Th1-type CD4 T cell immunity as an adjuvant for a tuberculosis vaccine.

The canine patient in the report was an eight-year-old, thirteen-kilogram spayed female Boston terrier with a soft, fluctuant, broad-based mass over her right elbow that had been slowly enlarging for approximately five months. Two cytological aspirates had yielded only adipose tissue, leading her veterinarians to initially suspect a benign lipoma. Because of the tumor’s size and location, complete surgical excision seemed unlikely, and incomplete removal of a soft tissue sarcoma typically condemns a dog to costly follow-up radiation. The owner, who happened to have long professional familiarity with TLR4 adjuvants, requested intratumoral EmT4™ injections before surgery in the hope of stimulating an anti-tumor immune response in place.

Two injections were given two weeks apart, each delivering 65 micrograms of EmT4™, equivalent to 5 micrograms per kilogram, a dose identical to that used in human trials of the related TLR4 agonist G100 in Merkel cell carcinoma and follicular lymphoma, and well below the 100-microgram-per-kilogram single dose of MPLA that research dogs tolerated without toxicity in earlier safety studies. Within hours of the first injection, the tumor swelled from roughly three to five centimeters, the overlying skin became taut, warm, and painful, and the dog became mildly lethargic, though she remained alert, responsive, and continued eating and drinking normally. The signs corresponded to a grade 1 adverse event under veterinary oncology criteria and resolved within a day. Notably, the second injection produced neither swelling nor discomfort, a pattern the authors attribute to the autoregulation that typically follows strong initial innate immune activation.

When the tumor was surgically excised four weeks after the second injection, histopathology confirmed a grade 2 soft tissue sarcoma, but with an unexpected feature: dense, tightly packed cuffs of immune cells encircled approximately half of the tumor’s blood vessels. Immunohistochemistry performed on the excised tissue revealed a heterogeneous immune infiltrate within these perivascular clusters, with CD20-positive B lymphocytes constituting the largest population at 57 percent, followed by CD3-positive T lymphocytes at 25 percent, Iba-1-positive macrophages and dendritic cells at 36 percent, FOXP3-positive regulatory T cells at just 8 percent, and CD204-positive macrophages at 5 percent. Two archived, non-injected soft tissue sarcomas of comparable grade and histology showed no CD3, CD20, or FOXP3 staining at all, and roughly threefold fewer Iba-1-positive cells, offering an informal point of comparison.

To probe the functional state of these infiltrating cells, the team employed RNAscope in situ hybridization, a technique that detects specific RNA transcripts within intact tissue sections. The results were striking: approximately 29 percent of cells in the lymphocyte clusters carried CD4 transcripts and 24 percent carried transcripts for tumor necrosis factor-alpha, the proinflammatory cytokine central to TLR4-driven inflammation, while 3.2 percent expressed the CD8 cytotoxic T cell marker and 1.3 percent carried interferon-gamma transcripts. The authors interpret the combination of clustered CD4 cells and abundant TNF-alpha as the signature of a Th1-biased immune response, the same profile observed in human soft tissue sarcoma patients treated with intratumoral GLA-SE and radiation. Given the short half-life of TNF-alpha protein and messenger RNA, its detection four weeks after the final injection suggests that immune activation was sustained up to the time of surgery.

The investigators are careful to emphasize the limitations of their observations. No pretreatment biopsy was available, because the mass had been presumed benign and was only sampled by non-diagnostic aspirates, so the team cannot prove that EmT4™ caused the immune infiltration rather than revealing a pre-existing one. Two archived tumors serve only as illustrative examples, not true controls. Canine soft tissue sarcomas are generally considered immunologically cold, owing to low mutational burdens and sparse neoantigen expression, and fibrosarcoma-type tumors in particular typically harbor few lymphocytes, which lends circumstantial weight to the idea that the agonist recruited the infiltrate. The authors also note that the immune cells remained concentrated in perivascular niches near the tumor periphery rather than penetrating its core, mirroring patterns seen in murine models where hypoxia and immunosuppressive factors in tumor interiors may block immune cell migration, and raising questions about whether differences in endothelial adhesion molecules dictate which vessels serve as entry points.

The clinical course of the patient offers a tantalizing coda. Although histology showed tumor cells extending to the surgical margins, the site was treated with two rounds of electrochemotherapy, and approximately thirty months later there has been no recurrence. The authors frame the case as foundational rather than conclusive, calling for controlled trials with pretreatment biopsies to establish appropriate dosing, toxicity profiles, and repeatability. Looking forward, they envision intratumoral EmT4™ as a component of combination regimens, potentially paired with immunogenic-cell-death-inducing radiation, low-dose cyclophosphamide to deplete regulatory T cells, or the veterinary immune checkpoint inhibitors now entering clinical use. In human medicine, intratumoral TLR4 agonists have already produced durable complete and partial remissions in Merkel cell carcinoma and abscopal tumor regressions in follicular lymphoma, with matching T cell clones detected in both tumors and circulating blood, evidence that local injection can seed systemic immunity. If controlled veterinary studies confirm what this single Boston terrier’s tumor suggested, the therapy could one day turn an ordinary vaccine adjuvant into a personalized, in situ cancer vaccine for dogs, and perhaps, by extension, a bridge to new approaches for human patients.

Subject of Research: Immunologic effects of intratumoral TLR4 agonist EmT4™ injection in a canine soft tissue sarcoma

Article Title: Preliminary immunologic observations of intratumoral EmT4™, a TLR4 agonist, in a canine soft tissue sarcoma

Article References: Helfand, S. C., Carossino, M., Kim, J., McMonigle Jr, D. R., Carter, D., & Gray, S. A. (2026). Preliminary immunologic observations of intratumoral EmT4™, a TLR4 agonist, in a canine soft tissue sarcoma. Veterinary Oncology, 3(1), Article 17. https://doi.org/10.1186/s44356-026-00063-6

Image Credits: AI Generated

DOI: 10.1186/s44356-026-00063-6

Keywords: TLR4 agonist, EmT4, monophosphoryl lipid A, intratumoral immunotherapy, canine soft tissue sarcoma, tumor microenvironment, TNF-alpha, veterinary oncology, perivascular immune niches, in situ vaccination, vaccine adjuvant, Boston terrier

Cellular senescence is a state in which a cell permanently stops dividing while remaining metabolically active. It is not the same as cell death. Senescence can arise when cells experience extensive DNA damage, oncogene activation, oxidative stress, shortened telomeres or exposure to cancer therapies. In healthy tissues, this response can act as a protective barrier by preventing damaged cells from continuing to proliferate. A senescent cell may also release signals that attract immune cells, allowing the immune system to identify and remove it. However, when senescent cells accumulate or escape immune clearance, the same biological program can become a source of chronic inflammation and tissue dysfunction.

The reason lies partly in the senescence-associated secretory phenotype, commonly known as SASP. Senescent cells can secrete inflammatory cytokines, chemokines, growth factors, proteases and other molecules that alter neighboring cells. Among the best-known signaling factors are interleukin-6 and interleukin-8, although the composition of SASP varies according to the cell type, the original stress and the surrounding tissue. These secretions can remodel the extracellular matrix, stimulate the recruitment of immune cells and influence blood-vessel formation. In a tumor, such signals may create conditions that support malignant-cell survival, invasion and resistance to treatment, even when the senescent cells themselves are no longer dividing.

The article presents senescence as a context-dependent process rather than an inherently beneficial or harmful event. Senescent cancer cells may stop proliferating temporarily after chemotherapy or radiation, but some can later escape this state or develop altered properties that contribute to relapse. Senescent stromal cells, including fibroblasts and endothelial cells, can also modify the tumor’s physical and chemical environment. Their secreted factors may increase tissue stiffness, disrupt normal barriers and provide cancer cells with signals that promote migration. At the same time, senescence can stimulate immune recognition, meaning that the outcome depends on whether immune surveillance is effective, suppressed or redirected by the tumor.

The immune microenvironment is therefore central to the story. Cytotoxic T lymphocytes and natural killer cells can recognize and eliminate stressed or senescent cells, while macrophages and other innate immune populations participate in their removal. Yet tumors frequently develop mechanisms that weaken these responses. Persistent SASP signaling may attract immunosuppressive macrophages, regulatory T cells or myeloid-derived suppressor cells, populations that can restrain effective anti-tumor immunity. Inflammatory signals may also produce immune exhaustion, a condition in which T cells remain present but gradually lose their ability to attack malignant cells. The result can be an environment where senescent cells survive long enough to influence tumor progression.

These interactions help explain why therapies designed to induce senescence produce mixed results. Forcing cancer cells into a non-dividing state can limit tumor expansion, but the remaining senescent population may continue releasing biologically active molecules. This has led to interest in “senolytic” strategies, which aim to selectively eliminate senescent cells, and “senomorphic” approaches, which attempt to suppress harmful SASP signaling without necessarily killing the cells. Neither strategy is universally applicable. Senescent cells can have different molecular profiles, and removing them indiscriminately could interfere with tissue repair or beneficial anti-tumor responses. The review emphasizes that treatment design will likely require identifying which senescent populations are present, what signals they produce and how immune cells respond to them.

The pan-cancer perspective is important because senescence and immunity do not behave identically in every malignancy. The same cytokine can have different effects depending on the tumor’s genetic background, tissue of origin and immune composition. In some cancers, senescence may strengthen immune surveillance and make malignant cells more visible to the immune system. In others, the accumulation of senescent stromal or immune cells may create a persistent inflammatory niche that favors tumor growth. Molecular features such as p53 and p16 pathways, DNA-damage responses, metabolic changes and chromatin remodeling can influence whether a cell enters stable senescence, undergoes apoptosis or adopts a reversible quiescent state. Distinguishing these states is essential because they may appear similar but require different therapeutic interventions.

The implications are particularly significant for glioblastoma. This brain tumor grows rapidly, infiltrates surrounding tissue and often returns despite surgery, radiation and chemotherapy. The central nervous system also contains a specialized immune environment shaped by the blood–brain barrier, resident microglia and restricted immune-cell trafficking. In glioblastoma, senescent tumor cells and senescent cells in the surrounding neural and vascular compartments could contribute to a microenvironment that supports invasion and treatment resistance. SASP factors may influence microglial behavior, alter communication between tumor cells and blood vessels, and promote inflammatory conditions that do not translate into effective tumor destruction. These possibilities make senescence–immune interactions a potentially important component of glioblastoma biology, although they also underline the need for disease-specific evidence.

A major message of the research is that future cancer treatment may need to target communication networks rather than isolated cell populations. Combining therapies that induce senescence with immune checkpoint inhibitors, senolytics or SASP-modulating drugs could theoretically produce stronger responses than any one approach alone. However, such combinations could also increase toxicity, provoke damaging inflammation or eliminate immune cells that are needed for tumor control. Reliable biomarkers will be required to determine the senescence state of individual tumors, measure SASP activity and identify immune populations that are helping or hindering treatment. Single-cell sequencing, spatial transcriptomics and advanced imaging could allow researchers to map these interactions directly inside tumors instead of treating the microenvironment as a uniform entity.

By linking broad cancer mechanisms with glioblastoma, Zhao and colleagues place cellular senescence within a larger view of tumor evolution: cancer progression is shaped not only by mutations that drive malignant growth, but also by the signals exchanged among damaged, aging, immune and cancerous cells. The review does not present senescence as a simple switch between protection and harm. Instead, it describes a changing biological state whose consequences depend on timing, location and immune context. Understanding that network could help researchers design therapies that preserve the protective functions of senescence while preventing its inflammatory and immunosuppressive effects. For glioblastoma and other difficult-to-treat cancers, that distinction may become central to turning the tumor microenvironment from an ally of disease into an obstacle to progression.

Subject of Research: Cellular senescence, the immune microenvironment, pan-cancer tumor progression and implications for glioblastoma.

Article Title: Interconnected roles of cellular senescence and the immune microenvironment in tumor progression: from pan-cancer mechanisms to glioblastoma implications

Article References:

Zhao, W., Zhang, P., Li, L. et al. Interconnected roles of cellular senescence and the immune microenvironment in tumor progression: from pan-cancer mechanisms to glioblastoma implications. Cell Death Discov. (2026). https://doi.org/10.1038/s41420-026-03284-8

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41420-026-03284-8

Keywords: Cellular senescence, senescence-associated secretory phenotype, immune microenvironment, tumor progression, glioblastoma, cancer immunology, SASP, senolytics, immune surveillance, tumor biology

Tumor-infiltrating lymphocytes are a crucial biomarker within several cancer types, particularly malignant melanoma, the deadliest form of skin cancer. These immune cells infiltrate the tumor microenvironment and play an essential role in modulating the body’s immune response against tumor cells. Traditionally, pathologists estimate the density and localization of TILs by visually examining stained tissue sections under microscopy. This information serves two main clinical purposes: assisting in accurate diagnosis and providing insight into how aggressive or advanced a patient’s cancer is likely to be. However, manual estimations are inherently subjective and prone to inter-observer variability, which can limit the reproducibility and reliability of prognostic assessments.

The research team thus embarked on a study to evaluate how an AI-based tool designed to quantify TILs could influence pathological evaluations. The AI was trained to analyze digitized images of stained melanoma tissue sections, automatically identifying and counting immune cells within or adjacent to the tumor. The study enrolled 98 participants, comprising pathologists and other researchers with experience in pathology image assessments. These individuals were split into two groups. The control group consisted exclusively of experienced pathologists who performed assessments in the traditional manner without AI assistance. The experimental group included pathologists and other research professionals who analyzed the same images but with the benefit of AI-generated quantifications of TIL presence.

Each participant reviewed 60 digital tissue images from melanoma patients, with all cases retrospectively selected, meaning patient outcomes and treatment histories were already known but blinded to the assessors. The core aim was to compare the reproducibility between human-only and AI-assisted assessments, as well as to determine which method more accurately correlated with the true clinical outcomes. Remarkably, the results demonstrated the AI-supported group’s assessments to be not only more reproducible—showing significantly less variability between different evaluators—but also more predictive of patient prognoses. This suggests that integrating AI into pathological workflows can substantially augment the diagnostic precision in melanoma cases.

Reproducibility in pathological assessments is a critical factor directly linked to medical safety and treatment planning. Variations in TIL quantification by different pathologists have historically posed challenges for consistent prognoses, which could inadvertently affect decisions regarding the aggressiveness of therapy. By leveraging AI to reduce this variability, healthcare providers may be able to rely on more standardized and objective biomarker evaluations, ultimately leading to more personalized and effective patient management strategies.

Beyond reproducibility, the study’s retrospective design allowed for comparison against actual patient outcomes that had been previously documented. The AI-assisted assessments showed a higher concordance with these outcomes, indicating better clinical validity. This is a vital indicator of the AI tool’s potential utility in real-world clinical settings. Such AI-driven analyses could assist pathologists by highlighting areas of interest within tissue samples or by providing quantitative data that substantiate their qualitative judgments.

Balazs Acs, associate professor at the Department of Oncology-Pathology at Karolinska Institutet and a clinical pathologist involved in the study, remarked on the clinical implications of this breakthrough. He noted that understanding the severity of a patient’s melanoma through tissue analysis is fundamental for guiding treatment—it informs decisions about how aggressively a tumor should be managed. The new AI tool offers a robust means to quantify the TIL biomarker, representing an important step toward integrating AI into routine diagnostic pathology.

While the results are highly encouraging, the researchers emphasize that additional studies are necessary to confirm the clinical utility and safety of this AI tool before it becomes a standard component of pathology practice. These validation studies would verify its performance across diverse patient populations, institutions, and varied clinical scenarios. Nonetheless, the findings mark an important milestone in the convergence of artificial intelligence and medical diagnostics, with the potential to reshape how oncologists and pathologists approach melanoma prognostication.

The careful collaboration of multidisciplinary researchers, including computer scientists, pathologists, and clinicians, played an instrumental role in successfully developing this AI technology. The study demonstrates the feasibility of deploying AI in complex medical tasks and underscores the importance of human-AI collaboration rather than full automation. The AI tool acts as an adjunct, assisting experts to reach more accurate and repeatable decisions that can benefit patient care.

Funding for this study was provided by prestigious bodies including the Swedish Society for Medical Research, Region Stockholm, and several grants from the U.S. National Institutes of Health. These investments underscore the global importance of advancing AI applications in cancer diagnostics and support for cutting-edge innovations in pathology.

As the medical community continues to explore the intersection of artificial intelligence and histopathology, studies such as this highlight the transformative potential of integrating advanced computational tools into clinical workflows. With further validation, AI-assisted pathology could soon become a vital component in the diagnosis and treatment monitoring not only for melanoma but also for other cancers where immune cell infiltration is a key prognostic factor.

In sum, this landmark study provides compelling evidence that AI-supported analysis of tumor-infiltrating lymphocytes enhances both the precision and reproducibility of skin cancer pathology. Such innovations pave the way for more accurate prognostic assessments, ultimately improving personalized therapy approaches for patients afflicted with malignant melanoma.

Subject of Research: Not applicable
Article Title: Analytical and Clinical Validity of Pathologist-read versus AI-Driven Assessments of Tumor-Infiltrating Lymphocytes in Melanoma: A Multi-Operator and Multi-Institutional Study
News Publication Date: 3-Jul-2025
Web References: http://dx.doi.org/10.1001/jamanetworkopen.2025.18906
References: Aung TN, Liu M, Su D, Shafi S, et al. Analytical and Clinical Validity of Pathologist-read versus AI-Driven Assessments of Tumor-Infiltrating Lymphocytes in Melanoma: A Multi-Operator and Multi-Institutional Study. JAMA Network Open, 2025.
Image Credits: Photo: Niklas Elmehed
Keywords: Artificial intelligence, Skin cancer, Tumor growth

HNSC, a malignancy notorious for its aggressive behavior and poor clinical outcomes, has long eluded comprehensive understanding in terms of molecular drivers influencing tumor growth and immune evasion. The current study leverages state-of-the-art bioinformatics coupled with rigorous in vitro experimentation to dissect the multifaceted functions of ADORA2B. By integrating data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), the investigators provide compelling evidence that ADORA2B expression is markedly elevated in tumor tissues relative to adjacent normal tissues, indicating its potential as a tumor-specific biomarker.

Crucially, ADORA2B expression correlates strongly with advanced clinical staging and worse patient prognoses, as evidenced by diminished overall survival (OS) and progression-free survival (PFS) metrics. These findings suggest a prognostic utility for ADORA2B, whereby its detection could inform clinical decision-making and herald more aggressive disease courses. Functional pathway analyses reveal that high levels of ADORA2B coincide with the downregulation of key immune-related signaling cascades, underscoring a molecular basis for tumor-mediated immune suppression.

The data from immune infiltration assessments highlight an alarming pattern: tumors exhibiting elevated ADORA2B display lower immune and stromal scores, indicative of an inhospitable environment for immune cell infiltration. This immunosuppressive tumor microenvironment (TME) is particularly challenging in cancer therapy, as it dampens the effectiveness of immune-mediated interventions including immune checkpoint blockade (ICB) therapies. Indeed, patients with heightened ADORA2B activity demonstrated a poorer clinical response to ICB, signifying that ADORA2B may serve as an underlying mechanism driving resistance to immunotherapy.

By employing weighted gene co-expression network analysis (WGCNA), the study further delineates the biological networks entwined with ADORA2B expression. These analyses spotlight key gene clusters and signaling pathways that mediate both tumor proliferation and immune evasion, offering insights that could catalyze the development of combinational treatments targeting ADORA2B alongside conventional immunotherapies.

The translational significance of this research is amplified by in vitro experiments involving siRNA-mediated knockdown of ADORA2B in HNSC cell lines. These cell-based assays—comprising cell viability (CCK-8), colony formation, and wound healing experiments—conclusively demonstrate that silencing ADORA2B hampers cancer cell proliferation and curtails migratory capabilities. Such findings not only validate the oncogenic role of ADORA2B but also spotlight its viability as a therapeutic target.

Beyond the cellular and molecular underpinnings, computational drug sensitivity analyses identify promising therapeutic candidates capable of counteracting ADORA2B-driven tumor dynamics. Compounds such as Ixazomib citrate and Masitinib emerge as potential agents with efficacy against high ADORA2B-expressing tumors, revealing a pharmacopeia that could be repurposed or further optimized in clinical settings.

This study’s integrative approach, blending comprehensive genetic datasets with functional biological validations, exemplifies the future of precision oncology. Understanding the dual influence of ADORA2B in fostering tumor growth and sculpting immune escape mechanisms provides a foundational platform for the development of novel diagnostics, prognostics, and therapeutics specifically tailored to combat HNSC.

The immunological context of ADORA2B’s role uncovers a complex interplay: while adenosine receptors have been widely implicated in immune modulation, ADORA2B appears particularly adept at silencing immune activation within tumors, thus fostering a “cold” TME that resists immune attack. The suppression of immune cell infiltration not only facilitates tumor growth but also poses a formidable barrier to immunotherapies, which rely on robust immune engagement.

Clinically, the stratification of patients based on ADORA2B levels offers an avenue for personalized medicine, whereby those exhibiting high receptor expression might benefit from combined therapeutic regimens that simultaneously inhibit ADORA2B and reinvigorate the immune system. This precision approach could significantly enhance response rates and overcome resistance observed with monotherapies.

Equally important is the identification of ADORA2B as a biomarker predictive of immunotherapy outcomes. As immune checkpoint inhibitors continue to reshape the oncology landscape, markers that forecast therapeutic efficacy are invaluable. This study positions ADORA2B as a potential gatekeeper biomarker, signifying which patients are less likely to respond to current immunotherapies and may require alternative or adjunctive treatments.

From a mechanistic standpoint, ADORA2B’s role as a G protein-coupled receptor (GPCR) situates it within a highly druggable class of proteins, many of which have been successfully targeted in other diseases. This pharmacological tractability accelerates the timeline for drug development, encouraging the exploration of ADORA2B antagonists or modulators in HNSC.

Moreover, the study’s implications transcend HNSC, encouraging researchers to consider ADORA2B’s involvement in other solid tumors characterized by immune evasive behaviors. The receptor’s influence on the tumor microenvironment signals a broader relevance to cancer biology, positioning ADORA2B as a linchpin in the interface between tumor progression and immune regulation.

Taken together, these multifaceted insights paint ADORA2B not simply as a molecular hallmark of tumor aggression but as a central orchestrator of immune suppression and therapeutic resistance. Targeting this receptor could redefine treatment paradigms in head and neck cancers, offering hope for improved survival and quality of life for patients who currently face limited options.

The findings also underscore the necessity of continued interdisciplinary research bridging bioinformatics, immunology, and molecular oncology. As researchers further unravel the ADORA2B signaling axis, novel combination therapies, including ADORA2B inhibitors with immune checkpoint blockade or standard chemotherapeutics, may emerge as potent cancer interventions.

In conclusion, the elucidation of ADORA2B’s role in HNSC marks a significant leap forward in comprehending the molecular and immunological intricacies underpinning this formidable cancer type. By advancing our understanding of tumor proliferation, migration, immune evasion, and treatment resistance, this research charts a promising course toward more effective diagnostic and therapeutic strategies. As the oncology community embraces these insights, the targeting of ADORA2B could soon translate from bench to bedside, transforming patient prognosis and heralding a new era in cancer care.

Subject of Research:

Article Title: ADORA2B promotes proliferation and migration in head and neck squamous cell carcinoma and is associated with immune infiltration

Article References:
Li, P., Pang, Kl., Chen, Sj. et al. ADORA2B promotes proliferation and migration in head and neck squamous cell carcinoma and is associated with immune infiltration. BMC Cancer 25, 673 (2025). https://doi.org/10.1186/s12885-025-14102-2

Image Credits: Scienmag.com

DOI: https://doi.org/10.1186/s12885-025-14102-2